Publisher Health

Scientists have recorded the first direct evidence that babies react differently to various smells and tastes while in the womb by looking at their facial expressions.
A study led by Durham University’s Fetal and Neonatal Research Lab, UK, took 4D ultrasound scans of 100 pregnant women to see how their unborn babies responded after being exposed to flavours from foods eaten by their mothers.
Researchers looked at how the fetuses reacted to either carrot or kale flavours just a short time after the flavours had been ingested by the mothers.
Fetuses exposed to carrot showed more “laughter-face” responses while those exposed to kale showed more “cry-face” responses.
Their findings could further our understanding of the development of human taste and smell receptors.
The researchers also believe that what pregnant women eat might influence babies’ taste preferences after birth and potentially have implications for establishing healthy eating habits.

A study by the Human Brain Project (HBP), led by scientists from the University of Liège (Belgium), has explored new techniques that may help distinguish between two different neurological conditions in patients with severe brain damage and or in a coma. The results of this study have just been published in open access in the journal eLife.
One of the greatest challenges in the field of neurology and critical care medicine is to correctly diagnose the level of consciousness of a patient in a coma due to a severe brain injury. Scientists at the Human Brain Project (HBP) — an international project involving more than 500 researchers that aims to gain a deeper understanding of the complex structure and function of the human brain through a unique interdisciplinary approach at the interface of neuroscience and technology — have been exploring new techniques that could help distinguish between two different neurological conditions.
The results of this new study, just published in the journal eLife, reveal important information about the mechanisms of consciousness disorders. The team of researchers from the University of Liège (GIGA Consciousness Research Unit, Coma Science Group, Faculty of Medicine) and the University Hospital of Liège (Belgium), the Universitat Pompeu Fabra (Spain), the Vrije Universiteit Amsterdam (Netherlands), among others, assessed the states of functional brain networks as a marker of consciousness in order to potentially distinguish between patients in unresponsive wakefulness syndromes (UWS) and the state of minimal consciousness (MCS).
“Previously known as the ‘vegetative state’, unresponsive arousal syndrome is the state of a patient who wakes up from coma, i.e. opens his or her eyes, but does not respond to the environment and verbal commands, showing only reflex movements,” explains Rajanikant Panda, first author of the paper and researcher at the GIGA Consciousness and Coma Science Group at ULiège. “In contrast, patients in a minimally conscious state show minimal signs of awareness such as following movements with their eyes or moving a finger when asked.” The differentiation of these states is essential for proper diagnosis, prognosis and rehabilitation treatment and is linked to important quality of life and even end-of-life decisions.
The study included 34 healthy controls, 30 minimally conscious patients and 14 unresponsive awake patients. These patients were sent from all over Europe to the Coma Science Group — led by neurologist Steven Laureys — and the University Hospital of Liege for a second opinion. Data sharing and analysis benefited from the EBRAINS infrastructure of the HBP and the collaboration of the study teams led by Jitka Annen (Coma Science Group/ ULiège Faculty of Medicine) and Prejaas Tewarie (Vrije Universiteit Amsterdam).
We used state-of-the-art techniques to assess different aspects of brain structure and its relationship to network dynamics,” says Jitka Annen, “and demonstrated that these techniques were sensitive in detecting clinically relevant differences in the diagnosis of patients with the minimally conscious state and unresponsive wakefulness syndrome.”
Specifically, the researchers used functional magnetic resonance imaging (fMRI) data to analyse dynamic functional connectivity, or how brain regions interact with each other, between neuronal populations and its association with structural white matter connections.
We observed that, compared to the minimally conscious state, patients with unresponsive wakefulness syndrome showed less activity in functional networks, reduced metastability (a state of stable functional connectivity different from the natural steady state) and increased coupling of functional connectivity to the structural framework,” explains Aurore Thibaut, FNRS researcher at GIGA Consciousness and Coma Science Group. “This new approach also revealed a brain network that most differentiates between unconscious and conscious states — a network encompassing subcortical regions and frontotemporoparietal cortical areas.”
These findings support previous ideas about the mechanisms underlying the loss and recovery of consciousness, such as the global neural workspace theory and the mesocircuit hypothesis, which suggest that the failure to recover consciousness is related to a loss of connectivity between subcortical and frontoparietal brain areas, as well as a loss of the range of functional network states.
“The study, funded in part by the HBP, the Belgian National Fund for Scientific Research (FNRS) and the Generet Prize of the King Baudouin Foundation, is a good example of how current theories of consciousness are challenged by real clinical neuroimaging data and how the knowledge generated translates into better patient care after severe brain injury,” concludes Jitka Annen, senior co-author of the paper and scientist at the GIGA Consciousness research unit.
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A team of scientists from the Singapore-MIT Alliance for Research and Technology (SMART), MIT’s research enterprise in Singapore,and Nanyang Technological University, Singapore (NTU Singapore) has developed a quick test kit that can tell if a person has immunity against COVID-19 and its variants, based on the antibodies detected in a blood sample.
Different from ART test kits — which look for the presence of viral proteins produced during a COVID-19 infection to determine if a person is infected — this rapid point-of-care test kit is a serology test that measures antibodies made by the patient. It requires a drop of blood and takes just 10 minutes to show results, as compared to the 24 to 72 hours required for conventional laboratory testing.
The test kit detects the levels of neutralising antibodies against SARS-COV-2, the virus causing COVID-19, and its variants such as Delta and Omicron, and can be easily adapted for new variants of concern and other diseases in the future.
Using a paper-based assay that is coated with chemicals that bind to antibodies in the blood sample, the test kit is low-cost, fast and has up to 93 per cent accuracy. It paves the way for personalised vaccination strategies, where people are only given vaccinations and booster shots when necessary, depending on their variance in antibody levels and immune response.
The findings were published in the scientific journal Microbiology Spectrum by the joint team led by SMART’s Antimicrobial Resistance (AMR) Interdisciplinary Research Group (IRG) and NTU’s School of Biological Sciences, in collaboration with Singapore’s National University Hospital (NUH) and National Centre for Infectious Diseases (NCID), and Massachusetts Institute of Technology (MIT).
The work is funded by the National Research Foundation (NRF) Singapore under its Campus for Research Excellence and Technological Enterprise (CREATE) programme. It is also supported by Singapore’s National Medical Research Council (NMRC), under its COVID-19 Research Fund, and National Health Innovation Centre (NHIC), under its COVID-19 Gap funding grant.

The advent of small-molecule targeted therapies, a decade ago, revolutionized the treatment of metastatic melanoma, provided that the tumors carry the mutations to respond to these treatments. However, despite a remarkable initial response that can be seen in a majority of patients, most of them will undergo relapse even after spectacular initial responses. These relapses are due to “dormant” persistent cells, unresponsive to treatment. A team from the University of Geneva (UNIGE) and the University Hospitals of Geneva (HUG) has shown that these cells under-express a protein called HuR. By deciphering the mechanism of this insufficient expression and by targeting it with an enzyme inhibitor, this team has succeeded in reducing the therapeutic resistance of all melanoma cells. These results, published in Biochemical and Biophysical Research Communications, open new therapeutic avenues against metastatic melanoma and other types of solid cancers.
Melanoma is one of the most dangerous skin cancers. Potentially very aggressive, it develops from melanocytes, the cells responsible for skin pigmentation. The initial tumor can be superficial with a good prognosis upon removal, it can also be deeper and become metastatic, i.e. migrate to other organs in the body.
For the last ten years, thanks to the advent of the so-called small-molecule targeted therapies — drugs that inhibit a precise mechanism within the tumor to fight it — half of the metastatic melanomas that carry a genetic signature making them sensitive to these drugs, can be treated effectively, sometimes even be eradicated. “However, despite such spectacular initial responses, 80% of patients will suffer recurrences, and these recurrences will often occur in the same initially affected sites,” explains Rastine Merat, researcher in the Department of Medicine at the UNIGE Faculty of Medicine and head of the Onco-dermatology Unit at the HUG.
A protein regulating cell division is involved
This phenomenon is called ”adaptive resistance”: certain cancer cells adapt to the drugs used to fight them and lead to a resurgence of the disease. This happens even when the metastases — and therefore the cells that make these tumors — seem to have completely disappeared. “This is explained by the persistence, after treatment, of small residues of so-called ‘dormant’ malignant cells that conventional radiology tools are unable to detect,” says Rastine Merat. “The particularity of these cells, in addition to being invisible, is that they proliferate slowly. This characteristic helps the cells to escape therapy, even during the initial treatment.”
Previously conducted research has shown that in slow-proliferating cells, a protein that among other things regulates the expression of many genes that control cell division — the HuR protein — is insufficiently expressed. This is in contrast with rapidly proliferating cells in which this protein is highly expressed. In a research work published in 2019, Rastine Merat and his team had established the link between the insufficient expression of this protein and the melanoma cells’ capacity to resist to a targeted therapy. In their recent research, they have uncovered a specific mechanism involved in the insufficient expression of this protein in the “dormant” cells that can be targeted with drugs.
Inhibiting enzymes to prevent recurrence
“In the cells, messenger RNAs play a central role in protein production. In the minority of cells in which HuR is insufficiently expressed, we found that the messenger RNAs of HuR were trapped by some other proteins. This is at least one of the mechanisms that causes HuR insufficient expression.” By using a chemical compound to inhibit two kinases — enzymes — involved in this mechanism, the UNIGE team managed to prevent HuR insufficient expression, reducing the ability of all melanoma cells to resist to treatment.
“The great difficulty in carrying out this work was to work on this type of cells, which are difficult to detect and analyze because of their small number and the fact that the state of insufficient expression of HuR protein is dynamic and reversible at any time for any cells; i.e. at any time the same cells can start to proliferate and flip to a state of high expression of this protein,” explains the researcher. To do this, “we paradoxically overexpressed this protein in melanoma cells. This allowed us to make the mechanisms at play more easily detectable.” This discovery opens new perspectives in the treatment of melanoma, but not only. “Melanoma is a model cancer: if we understand it, we can understand many other types of solid cancers,” explains Rastine Merat.
For the researcher and his team, “the next step will be to encourage the pharmaceutical industry to optimize the inhibitors of the identified kinases, — to improve their stability and bioavailability — which is something pharmaceutical drug companies know how to do nowadays in a very systematic way, at least for this type of target,” concludes Rastine Merat.
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A carbohydrate commonly found attached to plant proteins is a food source for the bacteria in our gut, new research suggests.
A paper published in the Proceedings of the National Academy of Sciences describes how species of gut microbes use plant N-glycans, a type of complex carbohydrate, as nutrients. The research was led by researchers from the University of Birmingham and Newcastle University, who used genomic data to identify specific enzymes produced by gut bacteria to break down the complex carbohydrate structures.
Information about enzymes that are produced by the gut microbiome will enable researchers to better understand how to manage good gut health. These enzymes also have biotechnological applications, such as reducing allergenic responses to food and some medicines. As the plant sugars that the gut microbes feed on are associated with some allergies from pollen and plant-based foods, the authors suggest that the enzymes could be harnessed to make some foods and medicines less likely to have allergic reactions.
Dr Lucy Crouch, lead author of the study from the Institute of Microbiology and Infection at the University of Birmingham said:
“The gut microbiome is an incredibly important feature for human health, and this finding will enable us to better understand the microbiome. By identifying the particular enzymes that these microbes use to digest their food, we can consider how future diets can be developed that promote a healthy gut, and as a result improve our general health.
“One unexpected outcome from the study is that insect N-glycans are also targeted by the some of the enzymes discovered. In a future scenario where we increasingly rely on alternative protein sources such as insects, this work provide insights into how insect proteins may also provide nutrients for our gut microbes.”
Dr David Bolam, co-lead author of the study from Newcastle University said: “We are still learning the role our gut plays in our overall health and so learning how microbes in our gut are able to use plant N-glycans is vital. This has developed our knowledge both in terms of understanding how these sugars are broken down by the microbiota, but also to discover new enzymes that could be used to alter and analyse N-glycan structures for medical and industrial applications.”
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A relatively large number of viruses can emerge from the clarinet. It releases considerably more aerosols, which can contain pathogens such as SARS-CoV-2, compared to other instruments such as the flute. However, the risk of transmission from an infected person on a wind instrument is generally much lower than for people who sing or speak, provided that one spends the same amount of time in their vicinity. This is the conclusion drawn by a research team from the Max Planck Institute for Dynamics and Self-Organization (MPI-DS) in Göttingen and the University Medical Center Göttingen (UMG) in a comprehensive study. The researchers determined the particle emission and the associated maximum risk of transmission when playing many different wind instruments. The results provide clues how cultural events can be organized with the lowest possible risk of infection, even during the pandemic.
The riskiest instrument is the voice, at least when it comes to spreading viruses such as SARS-CoV-2. Compared to breathing quietly, during singing or speaking infected people release more than 500 times particles into the air, which can contain viruses. When people play music with wind instruments, considerably less aerosol enters the environment than during singing — but still 5 to 50 times more than during breathing, as studied by a team led by Mohsen Bagheri and Eberhard Bodenschatz, director at the MPI-DS and professor at the Faculty of Physics at the University of Göttingen. Together with colleagues from the Institute of Hospital Hygiene and Infectiology at the UMG, the researchers analyzed how many particles of what size are released when 20 different wind instruments are played. They took the measurements under controlled conditions in a clean room and determined the upper limit for the risk of transmission with the omicron variant of SARS-CoV-2 from the results in each case. The study is available open access.
Risk of transmission depends on the instrument
“Surprisingly, we found that musical instruments are less risky than talking or singing,” says Mohsen Bagheri, head of a research group on aerosols at the MPI-DS. As the Göttingen team’s study shows, it is mainly the larger respiratory droplets, which are particularly important for the transmission of viruses, that remain trapped in wind instruments. The instruments thus act as a filter for larger particles. However, wind music is not harmless for the musicians and the audience from an infection protection point of view. This is due to the fact that particles with a size of less than five micrometers mostly emerge from the instrument. They remain in the air for a longer time and spread further, so that they can reach high concentrations, especially in unventilated rooms. The number of such small particles released by wind music also depends strongly on the instrument: While the team measured a very low concentration of released particles for various flutes, the measurements yielded values for the clarinet almost as high as for singing.
For example, at a distance of one and a half meters from a clarinet and trombone, the risk of transmission is already up to 50 percent after four minutes. Yet, at the same distance from a flute, this risk of transmission is only reached after three hours. All values for other instruments measured were in between.
Masks for instruments and people protect
In its study, the team also investigated how efficient the risk of transmission could be reduced by particle filters with similar properties to the fleece of FFP2 masks. They placed the prototype masks on the ends of brass instruments; woodwind instruments were almost completely encased in the filter material. “For brass instruments, an instrument mask reliably reduces the emission of infectious particles,” said Oliver Schlenczek, principal author of the study. If, in addition, the audience also wears an FFP2 mask, the risk of transmission is no more than 0.2 percent, even after one hour. Simone Scheithauer, Director of the Institute for Hospital Hygiene and Infectiology at UMG, considers these results to be very positive: “On this basis, we can recommend much more targeted protective measures in the future and maintain musical cultural activities with only minor restrictions even in critical situations,” she says.
“With adequate ventilation and the wearing of FFP2 masks, lessons, rehearsals and concerts with wind instruments can be conducted safely,” concludes aerosol researcher Eberhard Bodenschatz.

For decades, researchers from all over the world have been working hard to understand Alzheimer’s disease. Now, a collaboration between the Department of Biomedicine and the Department of Clinical Medicine at Aarhus University has resulted in a flock of minipigs that could lead to a major step forward in the research and treatment of Alzheimer’s.
The cloned pigs were born with a mutation in the gene SORL1, which is interesting because the mutations are found in up to 2-3% of all early onset Alzheimer’s cases in human beings.
Due to the gene mutation, the pigs develop signs of Alzheimer’s at a young age. This gives the researchers an opportunity to follow the early signs of the disease, as the pigs show changes in the same biomarkers that are used to make the diagnosis in humans.
“By following the changes over time in the pigs, we can better understand the earliest changes in the cells. Later, these changes lead to the irreversible alterations in the brain that are the cause of dementia. But now we can follow the pigs before they lose their memory, change their behaviour, etc., which will make it possible to test new drugs that can be used at an early stage to prevent SORL1-associated Alzheimer’s disease,” says Associate Professor Olav Michael Andersen, who is the first author of the study, which has just been published in the scientific journal Cell Reports Medicine.
“Pigs resemble human beings in many ways, which is why this increases the possibilities of producing drugs that will work to counteract Alzheimer’s. It is important to have a workable animal model to bridge the gap between research and drug development,” he explains.
Pigs cloned from skin cells
Since the 1990s, researchers have known of three genes which — if they mutate — can directly cause Alzheimer’s disease.

Two studies have revealed that certain disorders of the CAPRIN1 gene have significant consequences for people. First, the research team showed that insufficient production of the protein CAPRIN1 in the brain can lead to developmental differences, including autism spectrum disorders, attention deficit hyperactivity disorder (ADHD), and language disorders. Furthermore, the scientists identified a specific mutation in the CAPRIN1 gene (CAPRIN1P512L) that leads to an abnormal accumulation of proteins, causing unsteady gait and muscle weakness (myasthenia). The two studies have been published in the journals Brain and Cellular and Molecular Life Sciences.
These new insights were made possible by exome analyses, in which scientists observe which genes are altered in a cell. The team also used the GeneMatcher database — a platform on which researchers and physicians exchange information about mutations in genes and diseases associated with them.
The research team identified twelve patients who had mutations in the CAPRIN1 gene. In them, only half of the amount of protein was produced. Lisa Pavinato, a doctoral researcher in the team of Professor Dr Alfredo Brusco at the University of Turin and DAAD-scholarship holder with Professor Dr Brunhilde Wirth at the University of Cologne, discovered a connection between the deficient production of the protein and certain neurological impairments. The affected persons all had speech disorders, 82 per cent had ADHD, and 67 per cent were affected by autism spectrum disorders and other neurodevelopmental disorders. The function of CAPRIN1 was confirmed in laboratory experiments with human induced pluripotent stem cells in which the CAPRIN1 gene was switched off using the CRISPR/Cas9 technology, creating the conditions from which the affected individuals suffered. Cells with a CAPRIN1 mutation develop shortened processes and faulty circuits that show reduced electrical activity compared to the healthy neurons without the mutation. In contrast, control neurons without the CAPRIN1 mutation form long processes, developing into complex networks. Furthermore, the team also discovered changes in translation, one of the most important cellular processes for error-free cell formation and function. In fact, due to the faulty translation, the mutant neurons began to degenerate and form clumps after a few days. The results of this research have been published in the article ‘CAPRIN1 haploinsufficiency causes a neurodevelopmental disorder with language impairment, ADHD and ASD’ in Brain.
In the second study, GeneMatcher was used to identify three children from different families with a newly developed point mutation at a specific position of the CAPRIN1 gene: an amino acid exchange from proline to leucine at position 512. All three children show the same symptoms of early-onset movement disorders (ataxia), impaired speech motor skills (dysarthria), memory disorders, and myasthenia. Andrea delle Vedove, a doctoral researcher in the team of Professor Wirth, showed that this specific mutation leads to many protein clumps in neuronal cells similar to other neurodegenerative diseases such as Parkinson’s, Alzheimer’s or ataxia. In addition, the activity of the nerve cells was reduced. The study ‘CAPRIN1P512L causes aberrant protein aggregation and associates with early-onset ataxia’ has appeared in Cellular and Molecular Life Sciences.
‘The new research results are important not only for the affected patients and their families, who often spend years searching for answers to understand the cause of their disease, but also for physicians, who can now make faster and more accurate diagnoses,’ said Professor Dr Brunhilde Wirth, Director of the Institute of Human Genetics at University Hospital Cologne, who led the studies together with national and international teams.
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Researchers have developed a simple and fast way to perform optoretinography, an imaging technique that measures light-induced functional activity in the eye’s retina, the network of neurons in the back of our eyes responsible for detecting light and initiating vision. More than 50 percent of people in the U.S. over age 60 are affected by retinal diseases such as macular degeneration and diabetic retinopathy. These diseases affect the retina’s function in ways that reduce eyesight and can progress to blindness if not treated. The new approach could help accelerate the development of new treatments for eye diseases.
“Optoretinography has typically used very costly equipment that required multiple experts to operate while also producing enormous data volumes requiring extensive computational resources,” said research team leader Ravi Jonnal from the University of California, Davis. “We devised a way to do it more cheaper and quircker.”
Jonnal and colleagues report their new approach, which they call velocity-based optoretinography in Optica, Optica Publishing Group’s journal for high-impact research. They also demonstrate the method’s ability to measure retinal response in three healthy subjects.
“Although velocity-based optoretinography could potentially provide clinicians with more accurate and earlier information about functional losses in the retina, its first real impact is more likely to be in expediting clinical trials for new treatments of retinal diseases,” said Jonnal, who performed some of the first optoretinography measurements as a doctoral student in Don Miller’s lab at Indiana University. “If we can detect whether retinal function is getting better or worse faster than with traditional tests such as eye charts, it will greatly accelerate the development of treatments.”
Tracking shape changes
Optoretinography detects slight changes in the shape of neurons that generate or conduct signals in the retina. Until now, Jonnal and other investigators have used adaptive optics and optical coherence tomography (OCT) to visualize and track these neurons in the living, moving eye and then applied motion correction algorithms to stabilize the images and extract the functional response. This costly and time-consuming process requires resolving and tracking the position of individual cellular features and using those positions to determine whether the cell changed shape.
“When we use one of our adaptive optics systems to make optoretinography measurements, the experiment can easily take half a day and result in a terabyte of data that needs to be processed,” said Jonnal. “Processing the data to extract a functional signal takes, minimally, another day or two.”
To avoid the need to resolve and track individual neurons, Jonnal and colleagues wanted to see if they could instead measure the speed, or velocity, at which the retinal neurons move relative to each other. “We believed that even if the positions of the features vary from cell to cell, the speed at which they move relative to one another would be highly correlated among cells,” said Jonnal. “This proved to be correct.”
Measuring moving neurons
To carry out velocity-based optoretinography, the researchers developed a new OCT camera that allows a single operator to gather images from more locations in the retina than is possible with other approaches to optoretinography.
The researchers demonstrated their new technique by using it to collect measurements from three healthy volunteers. They were able to acquire data from each patient in just ten minutes and have that data processed and results available within 2 to 3 minutes. They showed that the functional optoretinographic responses measured with the simple approach scaled with the light stimulus dose used and that the dose-stimulus response was reproducible within and among the volunteers.
They are now planning experiments aimed at demonstrating the technique’s sensitivity to disease-related dysfunction. Jonnal is also working with clinicians at the University of California, Davis to use it for patient imaging and to aid in interpreting results for trials of stem cell therapies and gene therapy treatments for inherited retinal diseases. The researchers would also like to apply the new optoretinography approach to animal models of retinal disease.
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Omicron, the 13th named variant of the coronavirus, seems to have a remarkable capacity to evolve new tricks.Where is Pi?Last year, the World Health Organization began assigning Greek letters to worrying new variants of the coronavirus. The organization started with Alpha and swiftly worked its way through the Greek alphabet in the months that followed. When Omicron arrived in November, it was the 13th named variant in less than a year.But 10 months have passed since Omicron’s debut, and the next letter in line, Pi, has yet to arrive.That does not mean SARS-CoV-2, the coronavirus that causes Covid-19, has stopped evolving. But it may have entered a new stage. Last year, more than a dozen ordinary viruses independently transformed into major new public health threats. But now, all of the virus’s most significant variations are descending from a single lineage: Omicron.“Based on what’s being detected at the moment, it’s looking like future SARS-CoV-2 will evolve from Omicron,” said David Robertson, a virologist at the University of Glasgow.It’s also looking like Omicron has a remarkable capacity for more evolution. One of the newest subvariants, called BA.2.75.2, can evade immune responses better than all earlier forms of Omicron.For now, BA.2.75.2 is extremely rare, making up just .05 percent of the coronaviruses that have been sequenced worldwide in the past three months. But that was once true of other Omicron subvariants that later came to dominate the world. If BA.2.75.2 becomes widespread this winter, it may blunt the effectiveness of the newly authorized boosters from Moderna and Pfizer.Every time SARS-CoV-2 replicates inside of a cell, it might mutate. On rare occasions, a mutation might help SARS-CoV-2 replicate faster. Or it might help the virus evade antibodies from previous bouts of Covid.Such a beneficial mutation might become more common in a single country before fading away. Or it might take over the world.At first, SARS-CoV-2 followed the slow and steady course that scientists had expected based on other coronaviruses. Its evolutionary tree gradually split into branches, each gaining a few mutations. Evolutionary biologists kept track of them with codes that were useful but obscure. No one else paid much attention to the codes, because they made little difference to how sick the viruses made people.But then one lineage, initially known as B.1.1.7, defied expectations. When British scientists discovered it, in December 2020, they were surprised to find it bore a unique sequence of 23 mutations. Those mutations allowed it to spread much faster than other versions of the virus.Boosters that protect against the BA.5 subvariant are available, but experts worry BA.5’s dominance may be supplanted by another subvariant.Pfizer, via Associated PressWithin a few months, several other worrying variants came to light around the world — each with its own combination of mutations, each with the potential to spread quickly and cause a surge of deaths. To make it easier to communicate about them, the W.H.O. came up with its Greek system. B.1.1.7 became Alpha.Different variants experienced varying levels of success. Alpha came to dominate the world, whereas Beta took over only in South Africa and a few other countries before petering out.Read More on the Coronavirus PandemicA Blunted Response: Major data gaps, the result of decades of underinvestment in public health, have undercut the U.S. government’s response to Covid — and now to monkeypox.Biden’s Comments: In an interview that aired on CBS’s “60 Minutes,” President Biden said that “the pandemic is over.” But 400 to 500 Americans are still dying every day of Covid-19.Updated Boosters: As masks have fallen away and quarantines have diminished, the new vaccines are one of the last remaining weapons in America’s arsenal against the coronavirus. So far, the rollout is methodical, but muted.Educational Declines: Test results show the pandemic’s effect on U.S. students: The math and reading scores of 9-year-olds dropped steeply, erasing two decades of progress.What made the variants even more puzzling was that they arose independently. Beta did not descend from Alpha. Instead, it arose with its own set of new mutations from a different branch of the SARS-CoV-2 tree. The same held true for all the Greek-named variants, up to Omicron.It’s likely that most of these variants got their mutations by going into hiding. Instead of jumping from one host to another, they created chronic infections in people with weakened immune systems.Unable to mount a strong attack, these victims harbored the virus for months, allowing it to accumulate mutations. When it eventually emerged from its host, the virus had a startling range of new abilities — finding new ways to invade cells, weaken the immune system and evade antibodies.“When it gets out, it’s like an invasive species,” said Ben Murrell, a computational biologist at the Karolinska Institute in Stockholm.Omicron did particularly well in this genetic lottery, gaining more than 50 new mutations that helped it find new routes into cells and to infect people who had been vaccinated or previously infected. As it spread around the world and caused an unprecedented spike in cases, it drove most other variants to extinction.“The genetic innovations seen in Omicron were far more profound, as if it was a new species rather than just a new strain,” said Darren Martin, a virologist at the University of Cape Town.But it soon became clear that the name “Omicron” hid a complex reality. After the original Omicron virus evolved in the fall of 2022, its descendants split into at least five branches, known as BA.1 through BA.5.Over the next few months, the subvariants took turns rising to dominance. BA.1 went first, but it was soon outcompeted by BA.2. Each one was distinct enough from the others to evade some of the immunity of its predecessors. By this summer, BA.5 was on the rise.Getting a Covid test at an Esperanza Health Center in Chicago.Jamie Kelter Davis for The New York TimesThe U.S. Food and Drug Administration responded by inviting vaccine makers to produce booster shots that included a BA.5 protein along with one from the original version of the virus. Those boosters are now rolling out to the public, at a time when BA.5 is causing 85 percent of all Covid cases in the United States.But BA.5 could be fading in the rearview mirror by winter, scientists said. Omicron has continued to evolve — likely by sometimes jumping among hosts, and sometimes hiding for months in one of them.Since these new lineages belong to Omicron, they haven’t gotten a Greek letter of their own. But that doesn’t mean they’re just a slight twist on the original. Antibodies that could latch onto earlier forms of Omicron fare poorly against the newer ones.“They could arguably have been given different Greek letters,” Dr. Robertson said.BA.2.75.2 is among the newest of Omicron’s grandchildren, identified just last month. It’s also the most evasive Omicron yet, according to Dr. Murrell. In lab experiments, he and his colleagues tested BA.2.75.2 against 13 monoclonal antibodies that are either in clinical use or in development. It evaded all but one of them, bebtelovimab, made by Eli Lilly.They also tested the antibodies from recent blood donors in Sweden. BA.2.75.2 did substantially better at escaping those defenses than other Omicron subvariants did.The researchers posted their study online on Friday. Researchers at Peking University reached similar conclusions in a study posted the same day. Both have yet to be published in a scientific journal.Dr. Murrell cautioned that scientists have yet to run experiments that will show the effectiveness of BA.5 booster shots against BA.2.75.2. He suspected that getting a big supply of BA.5 antibodies would provide some protection, especially against severe disease.“It’s still important, but we’ll have to wait for the data to come out to see exactly what the magnitude of the boosting effect is,” Dr. Murrell said.There’s no reason to expect that BA.2.75.2 will be the end of the evolutionary line. As immunity builds to previous versions of Omicron, new versions will be able to evolve that can evade it.“I don’t think it’s going to hit a wall in the mutational space,” said Daniel Sheward, a postdoctoral researcher at the Karolinska Institute and co-author on the new study.Lorenzo Subissi, an infectious disease expert with the W.H.O., said that the organization was not giving Greek letters to lineages like BA.2.75.2 because they are much like the original Omicron viruses. For example, it appears that all Omicron lineages use a distinctive route to get into cells. As a result, it is less likely to lead to severe infections but possibly better able to spread than previous variants.“W.H.O. only names a variant when it is concerned that additional risks are being created that require new public health action,” Dr. Subissi said. But he did not rule out a Pi in our future.“This virus still remains largely unpredictable,” he said.